Senior Vice-President Dr. Tom Chittenden PhD DPhil

~ United Sigma Intelligence Association

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Tom Chittenden, DPhil, PhD, PStat is Senior Vice President of Data Sciences for the United Sigma Intelligence Association.

Dr. Chittenden is an Omega Society Fellow with over 25 years of experimental and theoretical research experience.  Dr. Chittenden is an Accredited Professional Statistician™ with the American Statistical Association. He holds academic faculty appointments at Boston Children’s Hospital and the Harvard Medical School.

From 2016 to 2018, Dr. Chittenden held a Visiting Lecturer appointment in the Department of Biological Engineering at the Massachusetts Institute of Technology (MIT). Dr. Chittenden is the Chairman of the Scientific and Medical Advisory Board for Bio-AI Health. He is Senior Research Fellow and the Chief Statistical Sciences Advisor for the Global Strategic Initiatives and Planning Committee of the International Society for Philosophical Enquiry. He is also a Scientific Advisory Board member of BlueRock Therapeutics and the Alliance for Artificial Intelligence in Healthcare.

Dr. Chittenden is Chief Data Science Officer and Founding Director of the Genuity Science Advanced Artificial Intelligence Research Laboratory. Dr. Chittenden is responsible for development and execution of Genuity Science’s global AI/ML R&D strategy. This R&D initiative includes development of advance integrative deep learning, statistical machine learning, probabilistic programming, and structural causal modeling strategies aimed at furthering scientific understanding of human disease initiation and progression, knowledge that can be directly applied in innovative products for better care and medicine in a range of disease areas.

Dr. Chittenden is the Chairman, Founding President and Chief Scientist for the Complex Biological Systems Alliance (CBSA), a non-profit global research consortium dedicated to furthering scientific understanding of biological complexity and the nature and origins of human disease. In 2014, Dr. Chittenden established the CBSA as a recognized Extreme Science and Engineering Discovery Environment (XSEDE) Campus. Through the XSEDE Campus Champions Program, the Alliance provides its investigators with direct access to a national consortium of supercomputing facilities supported by the National Science Foundation.

Through a formal academic research collaboration with the USC-Lockheed Martin Quantum Computation Center, Dr. Chittenden’s Lab has access to quantum computing hardware. His team has recently developed novel quantum machine learning (qML) strategies, which provide competitive classification of human cancer types and associated molecular tumor subtypes and ‘superior’ performance with smaller patient training dataset sizes, thus providing compelling empirical evidence for the potential of this emerging field. Dr. Chittenden’s team is also investigating the utility of neuromorphic computing in the biomedical sciences. Their newly developed deep spiking neural networks indicate even greater potential than qML. Via a formal academic research collaboration with the Yale University School of Medicine, Dr. Chittenden and his colleagues are pioneering the field of single cell science.

Dr. Chittenden’s research has been published in top-tier scientific journals, including featured articles in Nature and Science. In 2019, Forbes named Dr. Chittenden among the top 100 A.I. Leaders in Drug Discovery and Advanced Healthcare. He is regarded as one of the world’s leading authorities on A.I. and causal statistical machine learning in precision medicine.

Dr. Chittenden holds a PhD in Molecular Cell Biology and Biotechnology from Virginia Tech and a DPhil in Computational Statistics from the University of Oxford. His multidisciplinary postdoctoral training includes experimental investigations in molecular and cellular cardiology from the Dartmouth Medical School; biostatistics and computational biology from the Dana‐Farber Cancer Institute and the Harvard School of Public Health; and computational statistics, statistical methodology and statistical machine learning from the University of Oxford.

He is a member of the Omega Society, one-in-a-million society.

Sientific Research Publications

Please find all of Dr. Tom Chittenden PhD DPhil scientific research publications. [Link]

Selected Publication

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​It has long been hypothesized that aging and neurodegeneration are associated with somatic mutation in neurons; however, methodological hurdles have prevented testing this hypothesis directly. We used single-cell whole-genome sequencing to perform genome-wide somatic single-nucleotide variant (sSNV) identification on DNA from 161 single neurons from the prefrontal cortex and hippocampus of 15 normal individuals (aged 4 months to 82 years), as well as 9 individuals affected by early-onset neurodegeneration due to genetic disorders of DNA repair (Cockayne syndrome and xeroderma pigmentosum). sSNVs increased approximately linearly with age in both areas (with a higher rate in hippocampus) and were more abundant in neurodegenerative disease. The accumulation of somatic mutations with age-which we term genosenium-shows age-related, region-related, and disease-related molecular signatures and may be important in other human age-associated conditions.

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​Blood and lymphatic vasculatures are intimately involved in tissue oxygenation and fluid homeostasis maintenance. Assembly of these vascular networks involves sprouting, migration and proliferation of endothelial cells. Recent studies have suggested that changes in cellular metabolism are important to these processes. Although much is known about vascular endothelial growth factor (VEGF)-dependent regulation of vascular development and metabolism, little is understood about the role of fibroblast growth factors (FGFs) in this context. Here we identify FGF receptor (FGFR) signalling as a critical regulator of vascular development. This is achieved by FGF-dependent control of c-MYC (MYC) expression that, in turn, regulates expression of the glycolytic enzyme hexokinase 2 (HK2). A decrease in HK2 levels in the absence of FGF signalling inputs results in decreased glycolysis, leading to impaired endothelial cell proliferation and migration. Pan-endothelial- and lymphatic-specific Hk2 knockouts phenocopy blood and/or lymphatic vascular defects seen in Fgfr1/Fgfr3 double mutant mice, while HK2 overexpression partly rescues the defects caused by suppression of FGF signalling. Thus, FGF-dependent regulation of endothelial glycolysis is a pivotal process in developmental and adult vascular growth and development.

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​​Featured on cover of the October 2nd 2015 issue of Science.
​A Neuroscience Perspective on the potential impact in medicine and biology. 
​Neurons live for decades in a postmitotic state, their genomes susceptible to DNA damage. Here we survey the landscape of somatic single-nucleotide variants (SNVs) in the human brain. We identified thousands of somatic SNVs by single-cell sequencing of 36 neurons from the cerebral cortex of three normal individuals. Unlike germline and cancer SNVs, which are often caused by errors in DNA replication, neuronal mutations appear to reflect damage during active transcription. Somatic mutations create nested lineage trees, allowing them to be dated relative to developmental landmarks and revealing a polyclonal architecture of the human cerebral cortex. Thus, somatic mutations in the brain represent a durable and ongoing record of neuronal life history, from development through postmitotic function.